NEUROLEPTIC DRUGS CAUSE TRAUMATIC BRAIN INJURY
Families for the Ethical Psychiatric Treatment of Patients and Prisoners
It is long past time to identify neuroleptic drugs as a cause of
Traumatic Brain Injury (TBI)
CAUTION: ANYONE CURRENTLY TAKING NEUROLEPTIC DRUGS SHOULD CONSULT THEIR DOCTOR REGARDING THE INFORMATION IN THIS PAPER BEFORE ATTEMPTING TO CHANGE THEIR DRUG REGIMEN. IT IS EXTREMELY DANGEROUS TO ABRUPTLY STOP TAKING THESE DRUGS ONCE YOU HAVE BEEN TAKING THEM FOR ANY LENGTH OF TIME.
What are neuroleptic drugs and what do they do?
Most people are unfamiliar with the term neuroleptic because the drug companies do not like this name, which means ‘to seize the brain’, or ‘to seize the central nervous system’. This was the name first given to the class of drugs that exhibited the ability to sedate patients and create emotional indifference. Chlorpromazine (brand name: Thorazine) was the first of these drugs to appear on the market in the early 1950’s. By 1962, psychiatrists, encouraged by the drug companies, had begun to refer to neuroleptics by the term ‘antipsychotics’, a name which better suited the marketing practices of the pharmaceutical companies, already in full swing. Whereas ‘neuroleptic’ sounded threatening, who could be against ‘antipsychotics’? After all, anything that prevents psychosis must be, by definition, a good thing. But the problem is, the drugs do a lot more than just act on psychotic mental states, so the term antipsychotic is misleading, to say the least. For that reason, throughout this article, we will use the term neuroleptics, with the understanding that the reader may know these drugs as antipsychotics.
Currently, the known effects of neuroleptics on the brain are:
- blocking the D2 receptors in the dopamine pathways between nerve cells of various regions of the brain (dopamine is one of more than 60 known neurotransmitters, passing signals between brain neurons);
- causing the death of neurons in the cerebral cortex;
- reducing overall brain volume and increasing volume of the ventricles;
- enlarging of the thalamus and the striatum;
- increasing the density of glial cells and swelling of the prefrontal cortex;
- increasing the number of synapses and changes in the proportions and properties of the synapses in the brain cells, and;
- decreasing the number of glial cells and consequent decrease in the gray matter in the parietal lobe. (1)
The human body is designed to protect its vital organs. The brain is, arguably, the most vital of all our organs. It is protected not only by the skull and the cerebrospinal fluid but by the so-called blood-brain barrier designed to prevent invasion of the brain through the bloodstream. Neuroleptic drugs are designed to pierce the blood-brain barrier, and thus elude the body’s natural defense system. Once they have penetrated the barrier and changed neurotransmission between brain cells, neuroleptics set in motion a sequence of events in the brain known as adaptation. Taking a neuroleptic drug one time has very different effects from taking it repeatedly. Because most neuroleptics are prescribed for very long time periods, even for a lifetime, the brain adaptations become permanent structural changes with multiple effects.
Psychiatrists divide these effects into therapeutic effects and side effects, but this distinction is purely arbitrary and biased. For instance, reduced brain volume may be considered a side effect by the treating psychiatrist, but it is unlikely that patients will agree. It is more logical to consider the structural changes induced by neuroleptics as traumatic brain injury (TBI), a term now coming into vogue as soldiers returning home with head trauma, while fighting for medical benefits, have politicized this tragic occurrence. Injury to the brain, according to neurologists and psychiatrists, can occur as a result of physical force, electrical shock, emotional stress (post-traumatic stress disorder), or chemical invasion. There is no reason, other than adherence to prevailing medical orthodoxy, not to classify the adaptation of the brain to prescribed neuroleptic drugs as TBI. The reason this is not even considered by the medical establishment is that it would automatically mean that most current drug treatment of mental problems would be classified as iatrogenic treatment (harm caused to the patient by the psychiatrist).
As Joanna Moncrief has noted, people have a
“…need to believe in a cure for psychiatric conditions…and…(that)
is the strongest impetus behind the use of modern-day psychiatric
drugs…. It is difficult to overstate the central role that drug treatment
plays in modern-day psychiatry.” (2)
Drug companies have facilitated and played upon this desire for a cure to further the sale of their products. Through intensive marketing efforts, sponsored research, promoting their favorite advocacy groups, and misrepresentation of drug effects through various techniques like the name-change tactic noted above, the drug companies have succeeded to a large extent in bolstering the belief amongst the general populace that drugs are the premier treatment for mental disorders. Therefore, it is important to examine the real meaning of the changes in brain structure that are known to occur as a result of treatment with these drugs.
Some effects on brain function
What do the changes noted above mean in terms of brain function? Let’s look, for instance, at the changes in the glial cells in the pre-frontal cortex. Glial cells make up about 90% of the human brain and play the following roles in the brain and spinal cord (central nervous system):
(1) surround the neurons and hold them in place;
(2) supply nutrients and oxygen to the neurons;
(3) insulate neurons from each other, and;
(4) destroy pathogens and remove dead neurons.
From the above functions, we can infer that the increase in glial cells in the prefrontal cortex of the brain as a result of the presence of neuroleptic drugs would indicate that the neurons are under attack and in need of more nutrients, more protection from pathogens (the neuroleptic drugs), and removal of dead neurons (killed by the effects of the neuroleptics). Since the prefrontal cortex is the location of the higher level cognitive skills in the brain (planning, personality expression, decision making, and moderating social behavior), the increase in glial cells in this region would logically be connected to the decline in cognitive skills, flattened affect of the personality, poor decisions, and altered social behavior associated with the continuous use of neuroleptic drugs. In other words: neuroleptic drugs cause brain trauma, and this trauma can be directly related to symptoms commonly associated with, and indistinguishable from, mental illness. The fact that psychiatrists, the drug industry, academics, the legal system and the governmental bodies supposedly regulating the industry refuse to recognize this brain trauma as such is an indication of just how far a revolt against science has proceeded under the influence of the special interests dominating our current economic and political system.
But we have just begun to examine the many effects of neuroleptic drugs on the brain. Let’s look at another aspect – the effect of the drugs on the neurotransmitter dopamine. Dopamine performs numerous functions in the brain transmission system. It is well established, for instance, that Parkinson’s disease (PD) is caused by degeneration of dopamine neurons in the substantia nigra and a loss of dopamine in the putamen. Though described as a motor disease, PD also produces cognitive and behavioral symptoms. (3) In treating PD with the amino acid L-DOPA (levadopa – one of the building blocks of dopamine), a condition called Dopamine Dysegulation Syndrome (DDS) occurs after prolonged treatment. DDS is marked by self-control problems in the patient, like addiction or hypersexuality. (4) (Actually, the symptoms are the same as for mania, but, again, labels are important for the purposes of influencing public perception. It would not be helpful, from the drug companies’ standpoint, to admit that any [purportedly therapeutic] drug treatment can result in behavior related to psychosis). The diagnosis of DDS is clinical, since, like psychiatric diagnoses, there are no laboratory tests to confirm it. The only treatment available is to reduce or stop the administration of L-DOPA. (5) The question that naturally arises is this: if treatment with L-DOPA causes an adaptation in the brain resulting in behavioral symptoms akin to mental dysfunction, why is this possibility not considered in the case of treatment with neuroleptics for psychiatric diagnoses, which also cause brain adaptations in the dopaminergic system as a result of the treatment? Once again, as with the case of glial cell increase in the pre-frontal cortex noted above, this question has been virtually ignored by the psychiatric establishment. (6)
How science is being perverted
In scientific investigations, the most important question is what question to ask. In our present system, where most of the drug research is paid for by the drug companies themselves, the emphasis has to be on selling more products. Therefore, any question that may point to the fact that the drugs themselves may be causing problems is a question that won’t be asked, in general. This is just a reality, and it will, inevitably, lead to reasoning that is anti-scientific. Let’s look at an example of just how irrational that reasoning can become.
Treatment Advocacy Center is an organization that purportedly advocates for the rights of persons with mental problems. It is funded entirely by the Stanley Medical Research Institute (SMRI), a non-profit founded by Theodore Stanley, who made his money in direct marketing. The details and history of TAC and SMRI can be found in another paper by FEPTOPP. (7) In one of the papers published by TAC, the following statement is made:
“Schizophrenia and bipolar disorder are known (sic) to produce structural brain changes as part of the disease process, so it is reasonable to expect drugs that are effective in treating these diseases to do likewise.” (8)
The TAC reasoning process goes like this: (1) There are mental diseases that cause brain changes, and these brain changes result in the deviant behavior we observe; (2) We have a drug that also causes brain changes, therefore; (3) We believe that the brain changes caused by the drug will correct the deviant behavior caused by the brain changes caused by the disease.
The third statement is the hypothesis put forward by TAC (we will ignore, for the sake of argument, the fact that the first statement has not been proven). Scientific method demands that we have to ask of any hypothesis: How likely is this to be true? If it is not very likely, it is a poor hypothesis. TAC’s hypothesis has an infinitesimal likelihood of being true, given the nature of the brain, which is composed of billions of cells interacting with each other in ways that are far too complex for any model of our current understanding to imitate. The chance that any drug would act on the brain in such a way as to correct the behavior caused by the (unknown) supposed disease process is therefore mathematically so remote as to, effectively, be a zero possibility. Yet it is exactly this hypothesis that the current thrust of research funded by the drug companies pursues relentlessly. In fact, the opposite hypothesis is much more likely to be true. That is, if we believe that some mental illnesses cause brain changes and result in undesirable or unacceptable social behavior, then the likelihood is very great that further brain changes (caused by the drugs) will result in further altered behavior that also does not fall within acceptable social norms, since that is the phenomenon that we have already observed.
But this line of reasoning and these conclusions are obviously totally unacceptable to the status quo, regardless of the scientific validity of their premises. The nature of the relationships between the various entities that make up the psychopharmaceutical industrial complex (PPIC) make it (apparently) impossible for these questions to be tolerated or even suggested. (9) Although there are numerous intrepid individuals within the PPIC who have stepped forward with evidence to support alternative lines of reasoning (for which we are grateful and much indebted), these persons are marginalized within the PPIC and are assigned the role of conspiracy theorists. We have arrived at the historical point akin to when Galileo confronted the Pope. For the moment, the Pope prevails. But the opposition, based upon the truth and scientific method, will not melt away. It is largely the extent to which the status quo is wrong, together with the grave implications of admitting that error, that is currently preventing any serious consideration of the idea that TBI could result from neuroleptic drug treatment.
Other effects of neuroleptics
Many other cells in the body are also affected by the same neurotransmitters that affect brain function. Therefore, there are other effects caused by neuroleptic drugs. These include:
- toxicity to the heart, inducing conduction defects and arrhythmias;
- metabolic syndrome [obesity, diabetes, hypertension, pancreatitis, and dyslipidaemia (raised levels of cholesterol and blood lipids)];
- neuroleptic malignant syndrome [a potentially fatal condition in which the drugs appear to cause bodily temperature regulation centers to fail];
- sexual dysfunction;
- coronary heart disease.
The consequences of all this damage on persons subjected to long-term treatment with neuroleptic drugs are immense, long-term, destructive and permanent. Among these are:
- tardive dyskinesia [abnormal, involuntary repetitive movements, usually in the face and mouth, but also occurring in other muscles of the body];
- tardive dysmentia [unstable mood, loud speech, inappropriate body language, excessive emotional reactivity, enhanced responsiveness to environmental stimuli, reduced awareness of abnormal movements, heightened tension, aggression, mild elation];
- cognitive dysfunction [decline in intellectual capacity];
- decreased life expectancy;
- drug withdrawal syndrome [wherein the symptoms the drug was supposed to counteract actually become worse when the drug is withdrawn].
Why is TBI not currently identified with neuroleptic drug use?
The simple answer: Because the implications of prolonged neuroleptic drug exposure are dramatic, overwhelming, and have far-reaching consequences:
(1) Just like veterans returning with TBI, persons treated with neuroleptic drugs should automatically be eligible for disability benefits from various state and federal authorities. For instance, in California, Section 4358 of the Welfare and Institutions Code (W&IC) has recently created a Traumatic Brain Injury Fund in the State Treasury, to be used for:
“supported living services…community integration services…vocational
supportive services…(coordination of all) services needed by individuals
with TBI and their families…public and professional education…
prompt referral…and improvement of the system of services….”
W&IC 4354 defines “acquired traumatic brain injury” as “an injury that is sustained after birth from an external force to the brain or any of its parts, resulting in cognitive, psychological, neurological, or anatomical changes in brain functions.” It should be clear that neuroleptic drugs prescribed by a physician meet the criteria of “an external force” – but of course the existing PPIC will resist making this finding. The criteria that the drugs have caused “cognitive, psychological, neurological or anatomical changes in brain functions” is now already established beyond reasonable doubt.
W&IC 4362(a) notes that, “state public policy discriminates against adults with brain damage”, and W&IC 4362(f)(5) states, “the term ‘brain damage’ covers a wide range of organic and neurological disorders….These disorders include, but are not limited to…(p)ermanent brain damage…as a result of…substance toxicity….” (emphasis added);
(2) Psychiatrists prescribing neurolepticss may be liable for damages and medical censure due to iatrogenic practices (depending on the circumstances related to the prescription);
(3) Drug companies should be held liable for false advertising and cover-up of adverse neuroleptic drug effects;
(4) The Food and Drug Administration (FDA) bears direct responsibility for approving neuroleptic drugs and should be held accountable for adverse effects resulting from their use;
(5) Admitting that these drugs may cause behavior that can be dangerous and even violent would have far-reaching legal ramifications. Persons on trial for committing violent crimes who had been taking prescription neuroleptic drugs prior to the crime would have a legal argument that their behavior had been caused by the drugs, hence implicating the medical profession and the drug companies for legal culpability. The civil suits resulting from such rulings would be enormous and damaging to the drug companies’ public image;
(6) The fundamental paradigm of the PPIC’s claim that treatment of mental disorders is based upon ‘correcting a brain chemical imbalance’ would have to be rejected and new a theory or theories would need to be developed which undoubtedly would not rely on or benefit the pharmaceutical industry at the expense of other treatment modalities. In fact, it is already admitted, though not widely known, that the psychiatric explanation of a ‘biochemical imbalance’ in the brain as a cause of mental disorders is not true. (10) Brain research as far back as 1970 revealed that there was no ‘normal’ baseline for comparing chemical concentrations in the brain. (11) It is time for the psychiatric profession to drop this untruthful drug company marketing metaphor from their repertoire of medical methodology.
(1) Treatment Advocacy Center’s “Do antipsychotic drugs change brain structure?” found on the TAC website, www.treatmentadvocacycenter.org, downloaded 7/23/12. Also, see Note (2), pages 107-110.
(2) “The Myth of the Chemical Cure: A Critique of Psychiatric Drug Treatment”, by Joanna Moncrieff (Revised Edition), Palgrave MacMillan, 2009, pages 1, 2. Ms. Moncrieff is Senior Lecturer in the Department of Mental Health Sciences at University College, London, UK.
(3) “Dopaminergic modulation of cognitive function-implications for L-DOPA treatment in Parkinson’s disease”, Neuroscience Biobehavior Rev 30(1): 1-23, R. Cools, (2006).
(4) “Dopamine dysregulation syndrome, addiction and behavioral changes in Parkinson’s disease”, Parkinsonism Related Disorders 14 (4): 273-80, Merims D, Giladi N (2008).
(5) “Resolution of dopamine dysregulation syndrome following cessation of dopamine agonist therapy in Parkinson’s disease”, Journal of Clinical Neuroscience 15 (2): 205-8, Kimber TE, Thompson PD, Kiley MA, February, 2008.
(6) Op cit. Moncrief, p. 107.
(7) “On the Relationship Between NAMI, TAC and the Neo-Eugenics Movement”, FEPTOPP, (2012).
(8) Op cit. Treatment Advocacy Center, p. 1.
(9) For further information on the PPIC, see “Mental Health Care Manifesto”, FEPTOPP, 2012.
(10)See, e.g., “Psychiatry’s Grand Confession”, by Jonathan Leo, Ph.D. & Jeffrey Lacasse, Ph.D., posted on 1/23/12 at the website madinamerica.com.
(11)Rethinking Psychiatric Drugs”, Grace E. Jackson. M.D., Author House, 2005, p. 51.
As a class, neuroleptics are the most profitable drugs on the market. Neuroleptic drugs in use include the following (alphabetical partial list):
Chlorpromazine (Thorazine, Largactil)
Chlorprothixene (Cloxan, Taractan, Truxal)
Droperidol (Droleptan, Inapsine)
Flupenthixol (Depixol, Fluanxol)
Haloperidol (Haldol, Serenace)
Sertindole (Serdolect, Serlect)
Symbyax (Zyprexa and Prozac combined)
Zotepine (Nipolept, Losizopilon, Lodopin, Setous)
Zuclopenthixol (Cisordinol, Clopixol, Acuphase)